scholarly journals Association of the Insulinemic Potential of Diet and Lifestyle With Risk of Digestive System Cancers in Men and Women

2018 ◽  
Vol 2 (4) ◽  
Author(s):  
Weike Wang ◽  
Teresa T Fung ◽  
Molin Wang ◽  
Stephanie A Smith-Warner ◽  
Edward L Giovannucci ◽  
...  

Abstract Background We examined the role of the insulinemic potential of diet and lifestyle in the development of cancers of the digestive system, using two plasma C-peptide-based indices: the empirical dietary index for hyperinsulinemia (EDIH) and empirical lifestyle index for hyperinsulinemia (ELIH). Methods We used Cox regression to analyze data on 45 816 men (Health Professionals Follow-up Study, 1986–2012) and 74 191 women (Nurses’ Health Study, 1984–2012) to examine associations between EDIH and ELIH scores and digestive system cancers. We computed the diet-only score (EDIH) from food-frequency questionnaires administered every 4 years. The lifestyle score (ELIH) included diet, body mass index, and physical activity. Outcomes included incident cancer of the digestive system (mouth, throat, esophagus, stomach, small intestine, and colorectum) and its accessory organs (pancreas, gallbladder, and liver). P values were two-sided. Results We found direct associations between higher insulinemic potential of diet or lifestyle and risk of developing digestive system cancers in both men and women. The pooled multivariable hazard ratios (HRs) for participants comparing the highest to lowest EDIH quintile were: HR = 1.27, 95% confidence interval (CI) = 1.15 to 1.40, Ptrend < .001 for digestive system cancers; HR = 1.30, 95% CI = 1.17 to 1.45, Ptrend < .001 for digestive tract cancers (excluding accessory organs); and HR = 1.15, 95% CI = 0.93 to 1.41, Ptrend = .48 for digestive accessory organ cancers. The same associations were stronger with the lifestyle score: HR = 1.47, 95% CI = 1.23 to 1.76, Ptrend < .001 for digestive system cancers; HR = 1.49, 95% CI = 1.14 to 1.95, Ptrend = .001 for digestive tract cancers; and HR = 1.43, 95% CI = 1.17 to 1.73, Ptrend < .001 for digestive accessory organ cancers. Conclusions The findings suggest that interventions to reduce the insulinemic potential of diet and lifestyle may be a means of preventing digestive system cancer.

2020 ◽  
pp. 1-15
Author(s):  
Teresa R Haugsgjerd ◽  
Grace M Egeland ◽  
Ottar K Nygård ◽  
Jannicke Igland ◽  
Gerhard Sulo ◽  
...  

Abstract Objective: Limiting SFA intake may minimise the risk of CHD. However, such reduction often leads to increased intake of carbohydrates. We aimed to evaluate associations and the interplay of carbohydrate and SFA intake on CHD risk. Design: Prospective cohort study. Setting: We followed participants in the Hordaland Health Study, Norway from 1997–1999 through 2009. Information on carbohydrate and SFA intake was obtained from a FFQ and analysed as continuous and categorical (quartiles) variables. Multivariable Cox regression estimated hazard ratios (HR) and 95 % CI. Theoretical substitution analyses modelled the substitution of carbohydrates with other nutrients. CHD was defined as fatal or non-fatal CHD (ICD9 codes 410–414 and ICD10 codes I20–I25). Participants: 2995 men and women, aged 46–49 years. Results: Adjusting for age, sex, energy intake, physical activity and smoking, SFA was associated with lower risk (HRQ4 v. Q1 0·44, 95 % CI 0·26, 0·76, Ptrend = 0·002). For carbohydrates, the opposite pattern was observed (HRQ4 v. Q1 2·10, 95 % CI 1·22, 3·63, Ptrend = 0·003). SFA from cheese was associated with lower CHD risk (HRQ4 v. Q1 0·44, 95 % CI 0·24, 0·83, Ptrend = 0·006), while there were no associations between SFA from other food items and CHD. A 5 E% substitution of carbohydrates with total fat, but not SFA, was associated with lower CHD risk (HR 0·75, 95 % CI 0·62, 0·90). Conclusions: Higher intake of predominantly high glycaemic carbohydrates and lower intake of SFA, specifically lower intake from cheese, were associated with higher CHD risk. Substituting carbohydrates with total fat, but not SFA, was associated with significantly lower risk of CHD.


Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Luc Djousse ◽  
Andrew Petrone ◽  
John M Gaziano

Background: While previous studies have reported a positive relation of fried food consumption with type 2 diabetes, hypertension, and obesity, no previous study has examined the relation of total fried food intake with risk of heart failure (HF) in a prospective cohort. Objective: To test the hypothesis that fried food consumption is positively associated with risk of HF in male physicians. Methods: A prospective cohort of 19,968 participants from the Physicians’ Health Study. Frequency of fried food consumption was assessed between 1999 and 2002 using a food frequency questionnaire and HF was ascertained through annual follow-up questionnaires with validation in a subsample. We used Cox regression to estimate multivariable adjusted hazard ratios of HF. Results: During a median follow-up of 10.6 years, 862 cases of HF occurred. The mean age at baseline was 66.4 ± 9.2 years. Median frequency of fried food consumption was <1 time per week. Multivariable adjusted hazard ratios (95% CI) were: 1.0 (ref), 1.18 (1.01-1.37), 1.25 (1.02-1.54), and 1.68 (1.19-2.36) for fried food consumption of <1/week, 1-3/week, 4-6/week, and 7+/week, respectively (p for linear trend: 0.0004), after adjustment for age, alcohol use, smoking, exercise, and history of myocardial infarction, coronary artery bypass graph or angioplasty (Fig). Additional adjustment of total trans fats did not alter the findings. In a secondary analysis, body mass index did not modify the relation of fried foods with HF risk. Conclusions: Our data show a positive association between fried food intake and risk of HF in US male physicians.


Cephalalgia ◽  
2013 ◽  
Vol 34 (5) ◽  
pp. 327-335 ◽  
Author(s):  
Knut Hagen ◽  
Eystein Stordal ◽  
Mattias Linde ◽  
Timothy J Steiner ◽  
John-Anker Zwart ◽  
...  

Background Headache has not been established as a risk factor for dementia. The aim of this study was to determine whether any headache was associated with subsequent development of vascular dementia (VaD), Alzheimer’s disease (AD) or other types of dementia. Methods This prospective population-based cohort study used baseline data from the Nord-Trøndelag Health Study (HUNT 2) performed during 1995–1997 and, from the same Norwegian county, a register of cases diagnosed with dementia during 1997–2010. Participants aged ≥20 years who responded to headache questions in HUNT 2 were categorized (headache free; with any headache; with migraine; with nonmigrainous headache). Hazard ratios (HRs) for later inclusion in the dementia register were estimated using Cox regression analysis. Results Of 51,383 participants providing headache data in HUNT 2, 378 appeared in the dementia register during the follow-up period. Compared to those who were headache free, participants with any headache had increased risk of VaD ( n = 63) (multivariate-adjusted HR = 2.3, 95% CI 1.4–3.8, p = 0.002) and of mixed dementia (VaD and AD ( n = 52)) (adjusted HR = 2.0, 95% CI 1.1–3.5, p = 0.018). There was no association between any headache and later development of AD ( n = 180). Conclusion In this prospective population-based cohort study, any headache was a risk factor for development of VaD.


BMC Medicine ◽  
2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Heinz Freisling ◽  
Vivian Viallon ◽  
Hannah Lennon ◽  
Vincenzo Bagnardi ◽  
Cristian Ricci ◽  
...  

Abstract Background Although lifestyle factors have been studied in relation to individual non-communicable diseases (NCDs), their association with development of a subsequent NCD, defined as multimorbidity, has been scarcely investigated. The aim of this study was to investigate associations between five lifestyle factors and incident multimorbidity of cancer and cardiometabolic diseases. Methods In this prospective cohort study, 291,778 participants (64% women) from seven European countries, mostly aged 43 to 58 years and free of cancer, cardiovascular disease (CVD), and type 2 diabetes (T2D) at recruitment, were included. Incident multimorbidity of cancer and cardiometabolic diseases was defined as developing subsequently two diseases including first cancer at any site, CVD, and T2D in an individual. Multi-state modelling based on Cox regression was used to compute hazard ratios (HR) and 95% confidence intervals (95% CI) of developing cancer, CVD, or T2D, and subsequent transitions to multimorbidity, in relation to body mass index (BMI), smoking status, alcohol intake, physical activity, adherence to the Mediterranean diet, and their combination as a healthy lifestyle index (HLI) score. Cumulative incidence functions (CIFs) were estimated to compute 10-year absolute risks for transitions from healthy to cancer at any site, CVD (both fatal and non-fatal), or T2D, and to subsequent multimorbidity after each of the three NCDs. Results During a median follow-up of 11 years, 1910 men and 1334 women developed multimorbidity of cancer and cardiometabolic diseases. A higher HLI, reflecting healthy lifestyles, was strongly inversely associated with multimorbidity, with hazard ratios per 3-unit increment of 0.75 (95% CI, 0.71 to 0.81), 0.84 (0.79 to 0.90), and 0.82 (0.77 to 0.88) after cancer, CVD, and T2D, respectively. After T2D, the 10-year absolute risks of multimorbidity were 40% and 25% for men and women, respectively, with unhealthy lifestyle, and 30% and 18% for men and women with healthy lifestyles. Conclusion Pre-diagnostic healthy lifestyle behaviours were strongly inversely associated with the risk of cancer and cardiometabolic diseases, and with the prognosis of these diseases by reducing risk of multimorbidity.


2017 ◽  
Vol 23 (14) ◽  
pp. 1830-1838 ◽  
Author(s):  
Kjetil Bjørnevik ◽  
Tanuja Chitnis ◽  
Alberto Ascherio ◽  
Kassandra L Munger

Background: Results from previous studies on polyunsaturated fatty acid (PUFA) intake and multiple sclerosis (MS) risk are conflicting. Objective: To prospectively investigate the association between dietary intake of PUFA and MS risk. Methods: We followed 80,920 women from Nurses’ Health Study (1984–2004) and 94,511 women from Nurses’ Health Study II (1991–2009) who reported on diet using a validated food frequency questionnaire every 4 years and identified 479 incident MS cases during follow-up. We used Cox regression to estimate hazard ratios (HRs) and 95% confidence intervals (CIs), for the effect of PUFA intake on MS risk adjusting for age, latitude of residence at age 15, ancestry, cigarette smoking, supplemental vitamin D intake, body mass index, and total energy intake. Results: Higher intake of total PUFA at baseline was associated with a lower risk of MS (HR top vs bottom quintile: 0.67, 95% CI: 0.49–0.90, p trend = 0.01). Among the specific types of PUFA, only α-linolenic acid (ALA) was inversely associated with MS risk (HR top vs bottom quintile: 0.61, 95% CI: 0.45–0.83, p trend = 0.001). The long-chain fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were not associated with MS risk. Conclusion: Low dietary PUFA intake may be another modifiable risk factor for MS.


2011 ◽  
Vol 108 (7) ◽  
pp. 1307-1315 ◽  
Author(s):  
Diewertje Sluik ◽  
Heiner Boeing ◽  
Manuela M. Bergmann ◽  
Madlen Schütze ◽  
Birgit Teucher ◽  
...  

Studies have suggested that moderate alcohol consumption is associated with a reduced risk of CVD and premature mortality in individuals with diabetes mellitus. However, history of alcohol consumption has hardly been taken into account. We investigated the association between current alcohol consumption and mortality in men and women with diabetes mellitus accounting for past alcohol consumption. Within the European Prospective Investigation into Cancer and Nutrition (EPIC), a cohort was defined of 4797 participants with a confirmed diagnosis of diabetes mellitus. Men and women were assigned to categories of baseline and past alcohol consumption. Hazard ratios (HR) and 95 % CI for total mortality were estimated with multivariable Cox regression models, using light alcohol consumption (>0–6 g/d) as the reference category. Compared with light alcohol consumption, no relationship was observed between consumption of 6 g/d or more and total mortality. HR for >6–12 g/d was 0·89 (95 % CI 0·61, 1·30) in men and 0·86 (95 % CI 0·46, 1·60) in women. Adjustment for past alcohol consumption did not change the estimates substantially. In individuals who at baseline reported abstaining from alcohol, mortality rates were increased relative to light consumers: HR was 1·52 (95 % CI 0·99, 2·35) in men and 1·81 (95 % CI 1·04, 3·17) in women. The present study in diabetic individuals showed no association between current alcohol consumption >6 g/d and mortality risk compared with light consumption. The increased mortality risk among non-consumers appeared to be affected by their past alcohol consumption rather than their current abstinence.


2013 ◽  
Vol 31 (4_suppl) ◽  
pp. 514-514
Author(s):  
Allen Lee Cohn ◽  
Herbert Hurwitz ◽  
Tanios S. Bekaii-Saab ◽  
Johanna C. Bendell ◽  
Mark Kozloff ◽  
...  

514 Background: Randomized trials and OCSs have demonstrated that BV treatment in 1st-line (1L), in 2L, and across multiple lines is associated with longer survival in patients (pts) with mCRC. This analysis was aimed at comparing the effectiveness of BV after 1st disease progression (PD) between male and female mCRC pts who received 1L BV-containing therapy in a real-world setting. Methods: ARIES is a large, prospective OCS that enrolled pts who received BV and chemotherapy (CT) for 1L mCRC. Post-PD effectiveness was assessed for men and women characterizing BV use by cumulative and dichotomous approaches. The primary analysis treated BV exposure as cumulative BV doses after 1st PD and post-progression overall survival (ppOS) as the time from 1st PD to death. A time-dependent Cox regression model was fitted to assess the effect of cumulative BV exposure on ppOS, while controlling for potential confounders. A dichotomous secondary analysis characterized BV exposure as receipt of CT + BV (BBP) or CT alone (No BBP) within 2 months after PD and ppOS as time from 1st PD + 2 months to death. Results: Among the 1,550 1L mCRC pts enrolled, 1,199 (532 women) had PD. In the primary analysis, hazard ratios (HRs) for ppOS decreased, on average, by 1.2% with each additional BV dose. When stratified by sex, the average risk reduction per BV dose over 15 doses was 1.8% in women and 0.7% in men. In the secondary analysis that included 331 women (BBP, 180; No BBP, 151) and 417 men (BBP, 245, No BBP, 172) who received BV ± CT within 2 months post-PD, the HRs for ppOS with BBP treatment were 0.46 (95% CI, 0.35–0.59) in women and 0.52 (95% CI, 0.41–0.67) in men. Statistical interaction tests for differences in the effectiveness of BV between men and women were negative for primary and secondary analyses (P of 0.58 and 0.77). Protocol-specified adverse events occurred in 17.8% of women and 10.2% of men in the BBP population; this difference was largely related to rates of hypertension (8.3% vs 2.4%, respectively). Conclusions: In ARIES, the effectiveness of BV after first PD was not statistically different between women and men with mCRC. Clinical trial information: NCT00388206.


2016 ◽  
Vol 45 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Audun Brunes ◽  
W. Dana Flanders ◽  
Liv Berit Augestad

Aims: To examine the associations of self-reported visual impairment and physical activity (PA) with all-cause mortality. Methods: This prospective cohort study included 65,236 Norwegians aged ⩾20 years who had participated in the Nord-Trøndelag Health Study (HUNT2, 1995−1997). Of these participants, 11,074 (17.0%) had self-reported visual impairment (SRVI). The participants’ data were linked to Norway’s Cause of Death Registry and followed throughout 2012. Hazard ratios and 95% confidence intervals (CI) were assessed using Cox regression analyses with age as the time-scale. The Cox models were fitted for restricted age groups (<60, 60−84, ⩾85 years). Results: After a mean follow-up of 14.5 years, 13,549 deaths were identified. Compared with adults with self-reported no visual impairment, the multivariable hazard ratios among adults with SRVI were 2.47 (95% CI 1.94–3.13) in those aged <60 years, 1.22 (95% CI 1.13–1.33) in those aged 60–84 years and 1.05 (95% CI 0.96–1.15) in those aged ⩾85 years. The strength of the associations remained similar or stronger after additionally controlling for PA. When examining the joint associations, the all-cause mortality risk of SRVI was higher for those who reported no PA than for those who reported weekly hours of PA. We found a large, positive departure from additivity in adults aged <60 years, whereas the departure from additivity was small for the other age groups. Conclusions: Adults with SRVI reporting no PA were associated with an increased all-cause mortality risk. The associations attenuated with age.


Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Duck-chul Lee ◽  
Carl Lavie ◽  
Xuemei Sui ◽  
Steven Blair

Introduction: Obesity is a significant cardiovascular disease (CVD) risk factor. There is still little evidence, however, on the effects of resistance exercise (RE), independent of and combined with aerobic exercise (AE), on the development of obesity. Hypothesis: We hypothesised that RE, independent of AE, has significant benefits in obesity prevention. Methods: Participants were 12,583 men and women aged 18 to 89 years (mean age, 47) who received a preventive medical examination during 1987-2005 in the Aerobics Center Longitudinal Study. Participants were free of CVD, cancer, and obesity at baseline. RE, AE, and meeting the 2008 US Physical Activity Guidelines (RE ≥2 days/week and AE ≥500 MET-minutes/week) were determined by self-reported leisure-time exercise. Obesity was defined as body mass index of ≥30 mg/kg 2 using measured weight and height. Cox regression was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) of incident obesity by RE levels after adjusting for baseline age, sex, examination year, current smoking, heavy alcohol drinking, and meeting the AE guidelines. Results: During an average follow-up of 5.6 years, 919 (7.3%) developed obesity. Individuals meeting the RE guidelines (26%) had a 20% lower risk of developing obesity (HR: 0.80; 95% CI: 0.68 to 0.94) after adjusting for potential confounders and meeting the AE guidelines. The HRs (95% CIs) of incident obesity were 0.80 (0.60-1.05), 0.68 (0.52-0.88), 0.92 (0.68-1.26), and 0.84 (0.62-1.13) in weekly RE time of 1-59, 60-119, 120-179, and ≥180 minutes/week, respectively, compared with no RE. We found similar results in both men and women. In the combined analysis of RE and AE, HRs (95% CIs) of incident obesity were 0.65 (0.46-0.92) in meeting RE guidelines only, 0.72 (0.62-0.83) in meeting AE guidelines only, and 0.61 (0.51-0.73) in meeting both RE and AE guidelines, compared to meeting none of the guidelines. Conclusions: We found that RE, independent of and combined with AE, is associated with significantly lower risk of developing obesity, suggesting that RE should be added to habitual physical activity.


Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Andrew B Petrone ◽  
J. Michael Gaziano ◽  
Luc Djousse

Background: Previous studies have suggested that dark chocolate consumption may lower blood pressure, a major risk factor for heart failure. However, limited and inconsistent data are available on the association of chocolate consumption with the incidence rate of heart failure. Objective: To test the hypothesis that chocolate consumption is associated with a lower risk of heart failure. Methods: We prospectively studied 20,278 men from the Physicians’ Health Study. Chocolate consumption was assessed between 1999 and 2002 via a food frequency questionnaire and heart failure was ascertained through annual follow-up questionnaires with validation in a subsample. We used Cox regression to estimate multivariable adjusted relative risk of heart failure. Results: During a median follow-up of 9.3 years, there were 876 new cases of heart failure. The mean age at baseline was 66.4 ± 9.2 years. Median chocolate consumption was 1-3 times per month. Hazard ratios (95% CI) for heart failure were 1.0 (ref), 0.87 (0.73-1.04), 0.80 (0.66-0.98), and 0.87 (0.72-1.04), for chocolate consumption of less than 1/month, 1-3/month, 1/week, and 2+/week, respectively, after adjusting for age, body mass index (BMI), smoking, alcohol intake, exercise, and history of atrial fibrillation. In a secondary analysis, chocolate consumption was inversely associated with risk of heart failure in men whose BMI was <25 kg/m 2 but not in those with BMI of 25+ kg/m 2 ( Figure 1 ), p for interaction=0.0895. Conclusions: Our data suggest that moderate consumption of chocolate might be associated with a lower risk of heart failure, especially in lean individuals.


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